Jump to: Page Content, Section Navigation, Site Navigation, Site Search, Account Information, or Site Tools.
|
|
Sci. Signal., 14 April 2009 RESEARCHMechanical Signals Trigger Myosin II Redistribution and Mesoderm Invagination in Drosophila Embryos
Philippe-Alexandre Pouille*,
Padra Ahmadi*,
Anne-Christine Brunet, and
Emmanuel Farge UMR 168, CNRS, Institut Curie, 11 rue Pierre et Marie Curie, 75005 Paris, France. * These authors contributed equally to this work.
Abstract: During Drosophila gastrulation, two waves of constriction occur in the apical ventral cells, leading to mesoderm invagination. The first constriction wave is a stochastic process mediated by the constriction of 40% of randomly positioned mesodermal cells and is controlled by the transcription factor Snail. The second constriction wave immediately follows and involves the other 60% of the mesodermal cells. The second wave is controlled by the transcription factor Twist and requires the secreted protein Fog. Complete mesoderm invagination requires redistribution of the motor protein Myosin II to the apical side of the constricting cells. We show that apical redistribution of Myosin II and mesoderm invagination, both of which are impaired in snail homozygous mutants that are defective in both constriction waves, are rescued by local mechanical deformation of the mesoderm with a micromanipulated needle. Mechanical deformation appears to promote Fog-dependent signaling by inhibiting Fog endocytosis. We propose that the mechanical tissue deformation that occurs during the Snail-dependent stochastic phase is necessary for the Fog-dependent signaling that mediates the second collective constriction wave.
Citation: P.-A. Pouille, P. Ahmadi, A.-C. Brunet, E. Farge, Mechanical Signals Trigger Myosin II Redistribution and Mesoderm Invagination in Drosophila Embryos. Sci. Signal. 2, ra16 (2009). The editors suggest the following Related Resources on Science sites:In Science Signaling
|
Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882